Anterior Chamber

Published on 10/03/2015 by admin

Filed under Opthalmology

Last modified 10/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 5 (1 votes)

This article have been viewed 6039 times

6

Anterior Chamber

Primary Angle-Closure Glaucoma

Definition

Glaucoma due to obstruction of the trabecular meshwork by peripheral iris; classified as acute, subacute (intermittent), or chronic.

Etiology/mechanism
Pupillary Block

Most common. Lens–iris apposition interferes with aqueous flow and causes the iris to bow forward and occlude the trabecular meshwork.

Plateau Iris Syndrome (Without Pupillary Block)

Peripheral iris occludes the angle in patients with an atypical iris configuration (anteriorly positioned peripheral iris with steep insertion due to anteriorly rotated ciliary processes) (see Chapter 7).

Epidemiology

Approximately 5% of the general population over 60 years old have occludable angles, 0.5% of these develop angle-closure. Usually bilateral (develops in 50% of untreated fellow eyes within 5 years); higher incidence in Asians and Eskimos; female predilection (4 : 1). Associated with hyperopia, nanophthalmos, anterior chamber depth less than 2.5 mm, thicker lens, and lens subluxation.

Symptoms
Acute Angle-Closure

Pain, red eye, photophobia, decreased or blurred vision, halos around lights, headache, nausea, emesis.

Subacute Angle-Closure

May be asymptomatic or have symptoms of acute form but less severe; episodes evolve over the course of days or weeks and resolve spontaneously.

Chronic Angle-Closure

Asymptomatic; may have decreased vision or constricted visual fields in late stages.

Signs
Acute Angle-Closure

Decreased visual acuity, increased intraocular pressure, ciliary injection, corneal edema, anterior chamber cells and flare, shallow anterior chamber, narrow angles on gonioscopy, mid-dilated nonreactive pupil, iris bombé; may have signs of previous attacks including sector iris atrophy, anterior subcapsular lens opacities (glaukomflecken; due to lens epithelial cell ischemia and necrosis from high intraocular pressure), dilated irregular pupil, and peripheral anterior synechiae (PAS).

Subacute and Chronic Angle-Closure

Narrow angles; may have increased intraocular pressure, PAS, sector iris atrophy, glaukomflecken, optic nerve cupping, nerve fiber layer defects, and visual field defects.

Evaluation

 Complete ophthalmic history and eye exam with attention to pupils, cornea, tonometry, anterior chamber, indentation gonioscopy (Zeiss lens), iris, lens, and ophthalmoscopy.

 Check visual fields.

 Consider provocative testing (prone test, dark room test, prone dark room test, and pharmacologic dilation; intraocular pressure increase of >8 mmHg is considered positive).

Management

ACUTE ANGLE-CLOSURE

 Topical β-blocker (timolol [Timoptic] 0.5% q 15 min × 2, then bid), α-agonist (apraclonidine [Iopidine] 1% q 15 min × 2), and topical steroid (prednisolone acetate 1% q 15 minutes × 4, then q1h).

 Topical miotic (pilocarpine 1–2% min × 1 initially, then qid if effective; usually not effective if intraocular pressure > 40 mmHg due to iris sphincter ischemia; in 20% of patients pilocarpine will exacerbate the situation due to forward displacement of the lens–iris diaphragm); can also consider topical α-antagonist (thymoxamine 0.5% q 15 min for 2–3 hours).

 Systemic acetazolamide (Diamox 500 mg po STAT, then bid) and hyperosmotic (isosorbide up to 2 g/kg po of 45% solution).

 Laser peripheral iridotomy (LPI) with or without iridoplasty: Definitive treatment after acute attack is broken medically; may require application of topical glycerin (Ophthalgan) to clear corneal edema for adequate visualization of iris.

 Procedure parameters: A contact lens is used to stabilize the eye, focus the beam better, and place laser spots peripherally (in iris valley or crypt); patency of the iridotomy is confirmed by visualization of the lens capsule (often a rush of aqueous fluid through the hole is seen) not by the appearance of a red reflex.

 Argon laser (depends on iris pigmentation):

Dark brown: 0.02–0.05 s duration, 50 μm spot size, 600–1000 mW power; then 0.1 s and 400–600 mW through pigment epithelium.

Medium brown: 0.1–0.2 s duration, 50 μm spot size, 600–1000 mW power.

Blue: 0.05 s duration, 500 μm spot size, 200–500 mW power contraction burns; then 0.1 s duration, 50 μm spot size, 600–1000 mW power through stroma and 400–600 mW through pigment epithelium.

 Nd : YAG laser: 4–10 mJ power.

 Prophylactic laser peripheral iridotomy in fellow eye with narrow angle to prevent an acute attack in the future.

 If unable to perform laser peripheral iridotomy, consider surgical iridectomy.

 Consider goniosynechiolysis for recent peripheral anterior synechiae (< 12 months).

 Plateau iris syndrome may require long-term miotic therapy and peripheral iridectomy to reduce risk of pupillary block; consider argon laser iridoplasty or gonioplasty.

 Procedure parameters: 0.2–0.5 s duration, 200–500 μm spot size, 200–400 mW power, approximately 10 spot applications per quadrant, spots are placed on the iris as peripherally as possible and the power setting is adjusted until movement of the iris is observed.

SUBACUTE AND CHRONIC ANGLE-CLOSURE

 Laser peripheral iridotomy even without evidence of pupillary block.

 Treatment of increased intraocular pressure (see Primary Open-Angle Glaucoma section in Chapter 11); may require trabeculectomy or glaucoma drainage implant to lower pressure adequately.

Prognosis

Good if prompt treatment is initiated for acute attack; poorer for chronic cases but depends on extent of optic nerve damage and subsequent intraocular pressure control.

Secondary Angle-Closure Glaucoma

Definition

Acute or chronic angle-closure glaucoma caused by a variety of ocular disorders.

Etiology/mechanism
With Pupillary Block

Lens-induced (phacomorphic, dislocated lens, microspherophakia), seclusio pupillae, aphakic or pseudophakic pupillary block, silicone oil, nanophthalmos.

Without Pupillary Block

Posterior “pushing” mechanism

Mechanical or anterior displacement of the lens–iris diaphragm.

 Anterior rotation of ciliary body due to:

 Inflammation (scleritis, uveitis, panretinal photocoagulation).

 Congestion (scleral buckling, nanophthalmos).

 Choroidal effusion (hypotony, uveal effusion, medication [topiramate, sulfonamides]).

 Suprachoroidal hemorrhage.

 Aqueous misdirection (malignant glaucoma).

 Pressure from posterior segment (tumor, expanding gas, exudative retinal detachment).

 Developmental abnormalities (persistent hyperplastic primary vitreous, retinopathy of prematurity).

Anterior “pulling” mechanism

Adherence of iris to the trabecular meshwork or membranes over the trabecular meshwork.

 Epithelial (downgrowth or ingrowth).

 Endothelial (iridocorneal endothelial syndrome, posterior polymorphous dystrophy).

 Neovascular (neovascular glaucoma; see Chapter 7).

 Postinflammatory peripheral anterior synechiae.

 Adhesion from trauma.

 Mesodermal dysgenesis syndromes.

Symptoms
Acute Angle-Closure

Pain, red eye, photophobia, decreased or blurred vision, halos around lights, headache, nausea, emesis.

Chronic Angle-Closure

Asymptomatic; may have decreased vision or constricted visual fields in late stages.

Signs
Acute Angle-Closure

Decreased visual acuity, increased intraocular pressure, ciliary injection, corneal edema, anterior chamber cells and flare, shallow anterior chamber, narrow angles on gonioscopy, mid-dilated nonreactive pupil, iris bombé; signs of underlying etiology.

Chronic Angle-Closure

Narrow angles, increased intraocular pressure, PAS, signs of underlying etiology; may have sector iris atrophy, glaukomflecken, optic nerve cupping, nerve fiber layer defects, and visual field defects.

Evaluation

 Complete ophthalmic history and eye exam with attention to pupils, cornea, tonometry, anterior chamber, indentation gonioscopy, iris, lens, and ophthalmoscopy.

 Check visual fields.

Management

 Treat underlying etiology.

 Laser peripheral iridotomy for pupillary block.

 Topical cycloplegic (scopolamine 0.25% qid or atropine 1% bid) for malignant glaucoma, microspherophakia, after scleral buckle or after panretinal photocoagulation (do not use miotic agents).

 May require pars plana vitrectomy and lens extraction in refractory cases of malignant glaucoma or Nd : YAG laser disruption of the anterior hyaloid face in patient with pseudophakia and aphakia.

 Topical cycloplegic (scopolamine 0.25% qid), steroid (prednisolone acetate 1% qid), and panretinal photocoagulation for neovascular glaucoma.

 Cataract extraction may be necessary in some cases of lens-induced angle-closure glaucoma.

 Treatment of increased intraocular pressure (see Primary Open-Angle Glaucoma section in Chapter 11); may require trabeculectomy or glaucoma drainage implant to lower pressure adequately.

Prognosis

Poorer than primary angle-closure because usually due to chronic process; depends on etiology, extent of optic nerve damage, and subsequent intraocular pressure control.

Hypotony

Definition

Low intraocular pressure (≤ 5 mmHg).

Etiology
Increased Outflow (Excessive Drainage of Aqueous or Vitreous Fluid)

Trauma (cyclodialysis), surgery (wound leak, bleb overfiltration), choroidal effusion, retinal detachment.

Decreased Production (Ciliary Body Shutdown)

Inflammation (uveitis), medication (ciliary body toxicity: 5-fluorouracil, mitomycin-C, cidofovir, mannitol, anesthetic agents [fentanyl, succinylcholine, propofol, sevoflurane]), systemic disorder (bilateral hypotony: dehydration, ketoacidosis, uremia), cyclitic membrane, anterior proliferative vitreoretinopathy, ocular ischemic syndrome, phthisis.

Symptoms

Asymptomatic; may have pain and decreased vision.

Signs

Normal or decreased visual acuity, low intraocular pressure, functional and structural changes usually occur; may have refractive (hyperopic) shift, corneal folds and edema, positive Seidel test, filtering bleb, anterior chamber cells and flare, shallow anterior chamber, cyclodialysis cleft, cataract, cyclitic membrane, choroidal effusion, chorioretinal folds (hypotony maculopathy), cystoid macular edema, retinal detachment, proliferative vitreoretinopathy, optic disc edema, phthisis (end-stage; see Chapter 1).

Evaluation

 Complete ophthalmic history with attention to trauma, surgery, medications, and systemic conditions.

 Complete eye exam with attention to cornea, tonometry, anterior chamber, gonioscopy, and ophthalmoscopy.

 Seidel test (see Trauma: Laceration section in Chapter 5) to rule out open globe or wound leak in traumatic or postsurgical cases.

 B-scan ultrasonography to evaluate choroidal effusion, retinal detachment, and intraocular foreign body if unable to visualize the fundus.

 Consider ultrasound biomicroscopy (UBM) to identify cyclitic membrane, cyclodialysis cleft, and ciliary body detachment (≥ 2 clock hours).

 Consider fluorescein angiogram or OCT to identify choroidal folds.

Management

 Treat underlying etiology.

 Topical cycloplegic (cyclopentolate 1%, scopolamine 0.25%, atropine 1% bid to tid).

 Topical antibiotic for wound leak (gatifloxacin [Zymaxid] or moxifloxacin [Vigamox] qid).

 Bandage contact lens or pressure patch may work for small wound leaks.

 May require drainage of choroidal effusion or surgical repair of wound leak, retinal detachment, or ciliary body detachment.

 Consider Simmons’ shell or anterior chamber injection of viscoelastic or gas for bleb overfiltration.

 Steroids (topical, sub-Tenon’s, intravitreal, or oral), especially in cases due to uveitis.

 Consider topical ibopamine 2%.

Prognosis

Depends on etiology and duration.

Hyphema

Definition

Blood in the anterior chamber. Hyphema forms a layer of blood, whereas a microhyphema cannot be visualized with the naked eye (can only see red blood cells floating in the anterior chamber on slit-lamp examination).

Etiology

Usually traumatic (60% also have angle recession); may be spontaneous when associated with neovascularization of the iris or angle, iris lesions, or a malpositioned or loose intraocular lens (IOL).

Symptoms

Decreased vision; may have pain, photophobia, red eye.

Signs

Normal or decreased visual acuity, red blood cells in the anterior chamber (layer or clot); may have subconjunctival hemorrhage, increased intraocular pressure, rubeosis, iris sphincter tears, unusually deep anterior chamber, angle recession, iridodonesis, iridodialysis, cyclodialysis, and other signs of ocular trauma; may have iris lesion or pseudophacodonesis of IOL implant.

Differential Diagnosis

Trauma, uveitis–glaucoma–hyphema (UGH) syndrome, juvenile xanthogranuloma, leukemia, child abuse, postoperative, Fuchs’ heterochromic iridocyclitis, rubeosis irides.

Evaluation

 Complete ophthalmic history and eye exam with attention to cornea, tonometry, anterior chamber, iris, and ophthalmoscopy; wait 2–4 weeks to perform gonioscopy and scleral depression in traumatic cases.

 B-scan ultrasonography to rule out open globe if unable to visualize the fundus.

 Consider UBM to evaluate angle structures.

 Lab tests: Sickle cell prep and hemoglobin electrophoresis to rule out sickle cell disease.

Management

 Topical steroid (prednisolone acetate 1% up to q1h initially, then taper over 3–4 weeks as hyphema and inflammation resolve).

 Topical cycloplegic (scopolamine 0.25% or atropine 1% bid to tid).

 Consider aminocaproic acid ([Amicar] 50–100 mg / kg q4h).

 May require treatment of increased intraocular pressure (see Primary Open-Angle Glaucoma section in Chapter 11

Buy Membership for Opthalmology Category to continue reading. Learn more here